Polycystic Kidney disease.
I remember Dr Clarke advising us to nip down to the renal unit and feel some big kidneys. I thought to myself well what are the chances of me getting that. Oh sweet irony! First kidney I felt was in finals! But it went fine. The first questions I got asked was explain the applied anatomy and physiology of PCKD!
It got better from there though and a managed to pull out a few bits from the deepest recesses of my memory about other organs pckd affects and the genetics of it.
Kidney transplant
Very complicated renal history - has had CAPD, haemodialysis and a renal transplant. Asked all about chronic kidney disease and its management, the functions of the kidney, hyperparathyroidism, how to manage bipolar disorder in a patient with chronic kidney disease (random, I think the examiner was a psychiatrist!)
Kidney transplant due to reflux nephropathy Asked what the causes of renal failure in an adult are - pre, renal and post.
Asked the potential s/e of immuno-suppressive medication.
Asked to describe why this patient may have bone problems and cause of these problems- attempted to recite the whole calcium/phosphate/vit d cycle. Wish I had been slicker and doing this.
Polycystic kidneys.
Asked how the patient may have presented as a teenager.
What other organs are affected by this condition?
Patterns of inheritance.
How to treat the condition
Ask to inform patient of treatment options - dialysis and transplants.
Polycystic Kidney Disease "this man is under the care of the renal team, find out more". The examiners wanted to know what PCKD was, what the inheritance was, what complications and associated extrarenal problems they may get. They wanted an initial and a long term management plan. They then moved onto cauda equina syndrome and asked me for the signs and symptoms of this, red flags I would need to look out for, how cauda equina is different from spinal cord compression, what causes cauda equina, what would be the things I would look for on examination and immediate management plan. Then they asked me differentials for back pain. The explanation to the patient was to imagine he just had musculoskeletal pain and I was in A&E - I had to discharge him and explain signs he needed to look out for and to come back if he had them etc...
Polycystic Kidney Disease : What is PKD? What is the mode of inheritance?What other organs are affected (I couldn't remember anything but liver cysts!) Investigations and why? Stages of Chronic Kidney Disease? Symptoms of

chronic renal failure?nIndications for Dialysis? How would you manage such a patient as a GP? Explain to patient what the disease is and how it will affect them.
Polycystic kidney disease again an asymptomatic patient. NO symptoms watsoever just palpabale kidneys!! was asked about what polycystic kidney disease is, other organs it affects, how to investigate for it. then all about chronic renal failure signs and symptoms. the different types of dialysis.
Had to explain to the patient what polycystic kidney disease is
Polycystic Kidney Disease - PC back pain
I was asked about the red flags of back pain and to explain them to the patient
PCKD 
 Man sees a nephrologist - explore. Investigations and management of APKD. PTH axis so actions of Ca, Vit D and PTH. How to screen people with it. Explain renal replacement therapy to patient.
Chronic renal failure due to neonatal ureteric reflux, with hypertension, osteoporosis, three previous renal transplants, two fistulas, and a recent aortic valve replacement. Also probably lots of other things that I missed! This one was a bit of a nightmare, but the questioning afterwards was quite fair: causes of acute and chronic renal failure, complications of renal failure, immediate and late management, and management of hyperkalaemia. Then had to explain the side effects of steroids, which wasn’t too bad, as I’d basically done that the day before for the first case. Wish I’d gone over renal failure once more before the exam though!
Renal transplant
Exam: Abdomen
Opening line 'lady has had kidney transplant, find out more' Very nice lady who had had 3 transplants over many years with spells of CAPD and haemodialysis with AV fistula in situ in between transplants. Questions about causes of chronic renal failure, how to investigate UTI and chronic pyelonephritis in children, investigations for renal failure, calcium metabolism and pros and cons of types of dialysis. Asked to explain process of transplant including the actual logistics and basic surgical details, risks of rejection and need for long term immunosuppression and complications from this.

● Anatomy, genetics and physiology of Polycystic kidney disease?
○ Abdominal cavity, retroperitoneal, left kidney, below diaphragm posterior to spleen
(T12-L3), right kidney, below diaphragm posterior to liver (L1-L4), 10-15m long.
Blood supply: R/L renal artery and vein.
○ Mainly autosomal dominant, but some autosomal recessive
○ Defects in PKD genes, involved in calcium transport and cell cycle.
○ Cysts form in utero in nephron, and continue to grow, compress the neighboring renal parenchyma, causing progressive compromise of renal function.
● Functions of the kidney?
○ Excretion of wastes (nitrogenous and urea)
○ Acid-base homeostasis (hydrogen ions)
○ Osmolality regulation / Electrolytes (ADH and NaCl processing)
○ Blood pressure regulation (RAS, angiotensin 2, aldosterone, NaCl)
○ Hormone secretion (Erythropoietin, renin, Vit D activation)
● Acute renal failure presentation?
○ Rapid reduction (hours-days) in kidney function, as measured by serum creatinine, or based on a rapid reduction in urine output. Find and treat the precipitating cause.
○ Presentation: Fatigue, loss of appetite, headache, nausea and vomiting (acidosis), arrhythmia/palpitation (hyperkalaemia), SOB (pulmonary oedema + acidosis)
■ Prerenal: Hypovolaemia, shock, blood loss, severe dehydration, heart failure, renal artery stenosis.
■ Renal: Glomerulonephritis, tumour lysis syndrome, tubular necrosis (heavy metals/drugs/ischaemia), nephritis (antibiotics / NSAIDs).
■ Post-renal: prostatic hypertrophy, kidney stones, catheter obstruction, bladder stone, bladder/ureteral/renal malignancy.
● Chronic renal failure presentation / Complications?
○ Acidosis, muscle weakness, peripheral oedema, hypertension, pulmonary oedema, anaemia
○ Hyponatraemia: confusion, anorexia, headaches, cramps
○ Hypermagnesemia: respiratory depression, areflexia
○ Hyperkalaemia: muscle weakness, arrhythmia, chest pain
○ Renal bone disease: osteoporosis, osteomalacia, osteosclerosis, pathological fractures
○ Uraemia: itching, pericarditis, erectile dysfunction, nausea, diarrhoea, vomiting, peripheral neuropathy, platelet dysfunction, encephalopathy, fatigue
● Hyperparathyroidism?
○ Primary: Raised Ca2+ & PTH. Parathyroid gland problem causing over secretion, due to adenoma, hyperplasia or malignancy.
○ Secondary: Low Ca2+ & raised PTH. Physiological (i.e. not parathyroid gland) - seen in kidney disease, pancreatitis, small malabsorptive bowel disease
○ Tertiary: Markedly raised Ca2+ & PTH. Loss of Ca2+ sensitivity, caused by hyperplasia following prolonged secondary hyperparathyroidism.
● Other organs affected in PCKD?
○ Cerebral aneurysms, hepatic cysts, pancreatic cysts, cardiac valve disease (especially mitral valve prolapse), colonic diverticula, and aortic root dilatation.

● Stages of chronic kidney disease?
○ Stage 1: GFR > 90 + symptoms (haematuria)
○ Stage 2: GFR 60-90
○ Stage 3: GFR 30-60
○ Stage 4: GFR 15-30
○ Stage 5: GFR <15
● Red flags for back pain and cauda equina syndrome?
○ CES = LMN syndrome.
○ Saddle anaesthesia, urinary retention and incontinence, faecal incontinence due to reduced anal tone, sciatic leg pain, leg weakness, progressive weakness.
● PTH axis, actions of Ca, Vit D, PTH?
○ Vit D (AKA calcitriol): increases Ca2+ uptake from gut, renal tubules and bone via osteoclasts
○ PTH: Increases Ca2+ uptake from renal tubules, bone via osteoclasts, increased kidney Vit D
○ Calcitonin: Decreases osteoclast activity, decreases Ca2+ intestinal absorption, decreases Ca2+ and PO4 reabsorption in proximal tubule.
● Pros and cons for different types of dialysis?
○ Peritoneal
■ Pros: done at home, more mobility, cheaper
■ Cons: SBP, bowel perforation, compressive symptoms (diaphragmatic splinting, constipation, urinary symptoms), peritoneal sclerosis and obstruction, not as efficient at toxin removal as haemodialysis.
○ Haemodialysis
■ Pros: Superior toxin removal, superior blood pressure control, lower mortality.
■ Cons: Expensive, inhibits travel and mobility, frequent hospital visits.
● How to tell the difference between kidney/bowel and kidney/spleen?
○ Kidney is ballottable, spleen is not
○ Notch on the anterior border is palpable in spleen, not in kidney
○ Spleen enlarges diagonally towards RLQ, while the kidney enlarges inferiorly
○ Upon deep palpation, the upper edge of spleen is not palpable, upper edge of kidney is
○ On auscultation, there can be a splenic rub upon breathing, whereas there is no renal rub.
● ECG signs of hyperkalaemia?
○ Tented T-waves, flattened p-waves, widened QRS
● Renal osteodystrophy?
○ Those with CKD cannot excrete PO4 or Mg2+
○ Thus Ca2+ not absorbed well.
○ Cannot convert Vit D into active form
○ PTH cannot act on kidney
○ Renal osteodystrophy occurs (bone pain and pathological fractures)
■ Hyperparathyroidism
■ Hyperphosphataemia

■ Hypocalcaemia